Wednesday, April 28, 2010

Grains as Food: an Update

Improperly Prepared Grain Fiber can be Harmful

Last year, I published a post on the Diet and Reinfarction trial (DART), a controlled trial that increased grain fiber intake using whole wheat bread and wheat bran supplements, and reported long-term health outcomes in people who had previously suffered a heart attack (1). The initial paper found a trend toward increased heart attacks and deaths in the grain fiber-supplemented group at two years, which was not statistically significant.

What I didn't know at the time is that a follow-up study has been published. After mathematically "adjusting" for preexisting conditions and medication use, the result reached statistical significance: people who increased their grain fiber intake had more heart attacks than people who didn't during the two years of the controlled trial. Overall mortality was higher as well, but that didn't reach statistical significance. You have to get past the abstract of the paper to realize this, but fortunately it's free access (2).

Here's a description of what not to eat if you're a Westerner with established heart disease:
Those randomised to fibre advice were encouraged to eat at least six slices of wholemeal bread per day, or an equivalent amount of cereal fibre from a mixture of wholemeal bread, high-fibre breakfast cereals and wheat bran.
Characteristics of Grain Fiber

The term 'fiber' can refer to many different things. Dietary fiber is simply defined as an edible substance that doesn't get digested by the human body. It doesn't even necessarily come from plants. If you eat a shrimp with the shell on, and the shell comes out the other end (which it will), it was fiber.

Grain fiber is a particular class of dietary fiber that has specific characteristics. It's mostly cellulose (like wood; although some grains are rich in soluble fiber as well), and it contains a number of defensive substances and storage molecules that make it more difficult to eat. These may include phytic acid, protease inhibitors, amylase inhibitors, lectins, tannins, saponins, and goitrogens (3). Grain fiber is also a rich source of vitamins and minerals, although the minerals are mostly inaccessible due to grains' high phytic acid content (4, 5, 6).

Every plant food (and some animal foods) has its chemical defense strategy, and grains are no different*. It's just that grains are particularly good at it, and also happen to be one of our staple foods in the modern world. If you don't think grains are naturally inedible for humans, try eating a heaping bowl full of dry, raw whole wheat berries.

Human Ingenuity to the Rescue

Humans are clever creatures, and we've found ways to use grains as a food source, despite not being naturally adapted to eating them**. The most important is our ability to cook. Cooking deactivates many of the harmful substances found in grains and other plant foods. However, some are not deactivated by cooking. These require other strategies to remove or deactivate.

Healthy grain-based cultures don't prepare their grains haphazardly. Throughout the world, using a number of different grains, many have arrived at similar strategies for making grains edible and nutritious. The most common approach involves most or all of these steps:
  • Soaking
  • Grinding
  • Removing 50-75% of the bran
  • Sour fermentation
  • Cooking
But wait, didn't all healthy traditional cultures eat whole grains? The idea might make us feel warm and fuzzy inside, but it doesn't quite hit the mark. A recent conversation with Ramiel Nagel, author of the book Cure Tooth Decay, disabused me of that notion. He pointed out that in my favorite resource on grain preparation in traditional societies, the Food and Agriculture Organization publication Fermented Cereals: a Global Perspective, many of the recipes call for removing a portion of the bran (7). Some of these recipes probably haven't changed in thousands of years. It's my impression that some traditional cultures eat whole grains, while others eat them partially de-branned.

In the next post, I'll explain why these processing steps greatly improve the nutritional value of grains, and I'll describe recipes from around the world to illustrate the point.

* Including tubers. For example, sweet potatoes contain goitrogens, oxalic acid, and protease inhibitors. Potatoes contain toxic glycoalkaloids. Taro contains oxalic acid and protease inhibitors. Cassava contains highly toxic cyanogens. Some of these substances are deactivated by cooking, others are not. Each food has an associated preparation method that minimizes its toxic qualities. Potatoes are peeled, removing the majority of the glycoalkaloids. Cassava is grated and dried or fermented to inactivate cyanogens. Some cultures ferment taro.

** As opposed to mice, for example, which can survive on raw whole grains.

Friday, April 23, 2010

Have Seed Oils Caused a Multi-Generational Obesity Epidemic?

In 2006, Drs. Gerard Ailhaud and Philippe Guesnet hypothesized that industrial seed oils such as corn, soybean, safflower, sunflower and cottonseed oil are at least partially responsible for the current obesity epidemic (1). These oils were not a significant part of the human diet until very recently, yet they have been promoted due to their supposed ability to prevent cardiovascular disease. The Western world has been living a massive uncontrolled experiment ever since.

Linoleic acid is an omega-6 polyunsaturated fatty acid (PUFA) that makes up a large proportion of seed oils.
It's a very bioactive molecule, in part because it's the precursor of two classes of signaling molecules (eicosanoids and endocannabinoids), some of which influence the development of fat tissue and regulate appetite.

Dr. Ailhaud and his colleagues pointed out that not only are people eating far more linoleic acid than ever before; that very same linoleic acid is accumulating in our fat tissue and showing up in breast milk. Here are a few graphs to illustrate the point. The first graph is of PUFA consumption in the US over the last century, primarily reflecting seed oil intake (based on USDA food disappearance records):

Here's a graph of added fat intake based on USDA data. Added animal fats such as butter and lard have remained stable since 1970 (although total animal fat intake has declined), while seed oil consumption has gone from high to higher:

The following graph shows linoleic acid accumulation in human body fat over the last few decades in Western nations (mostly the US). I put this together based on two references (2, 3). I didn't find any data from the US past 1986. Linoleic acid, unlike most other fatty acids, accumulates disproportionately in body fat (4):

And finally, linoleic acid in the breast milk of US mothers, from Dr. Ailhaud's 2006 paper (the black dots):

In 2009, Dr. Ingeborg Hanbauer published a paper showing that when mice are fed a diet with a poor omega-6:3 balance (77:1), after three generations they develop adult obesity (5). Mice fed the same diet with a better omega-6:3 balance (9.5:1) did not develop obesity, and remained smaller overall. This shows that PUFA imbalance can cause multi-generational effects resulting in obesity and excessive tissue growth. Cmdr. Joseph Hibbeln, a collaborator of Dr. Bill Lands, was an author. The thing I don't like about this paper is they didn't quantify the obesity by measuring fat mass, so we have to take the authors' word that they had more fat.

This week, Dr. Florence Massiera and collaborators published a similar paper titled “A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations” (6). Drs. Ailhaud and Guesnet were both on this paper. They showed that a 35% fat diet with an omega-6:3 ratio of 28 caused obesity that progressively increased over four generations of mice. Although this study was more detailed than the study by Dr. Hanbauer and colleagues, it lacked a comparison group with a more favorable omega-6:3 balance to show that the obesity was specifically the result of omega-6:3 imbalance, rather than the fact that the diet was higher in fat overall or some other aspect of its composition.

Both studies have serious problems. Nevertheless, together they suggest that PUFA imbalance is capable of causing obesity in mice that worsens over several generations.

If this is true in humans, it would be a straightforward explanation for the obesity epidemic that has plagued the Western world in recent decades. It would explain why the epidemic began in children around 1970, but didn’t show up in adults until about 1980. It would explain why the epidemic is less severe in Europe, and even less so in Asia. And of course, it correlates well with trends in seed oil consumption. This graph is based on US NHANES survey data:

We already know that a number of prenatal factors can have an effect on adult body fat levels in rodents, and observational studies have suggested that the same may apply to humans. If a mother’s body fat is full of linoleic acid, she will pass it on to the fetus as it grows, and after birth in breast milk, influencing its development.

As long-time followers of Whole Health Source know, I suspect industrial seed oils contribute to many of our modern ills. I can’t say for sure that seed oils are responsible for the current obesity epidemic, but the evidence certainly gives me pause. In any case, seed oils are an unnatural part of the human diet and it won’t hurt anyone to avoid them. The half-life of linoleic acid in fat tissue is about two years, so reducing it is a long-term prospect.

Sunday, April 18, 2010

Dinner with Taubes, Eades and Hujoel

Gary Taubes gave a lecture at UW last Thursday. Thanks to all the Whole Health Source readers who showed up. Gary's talk was titled "Why We Get Fat: Adiposity 101 and the Alternative Hypothesis of Obesity". He was hosted by Dr. Philippe Hujoel, the UW epidemiologist and dentist who authored the paper "Dietary Carbohydrates and Dental-Systemic Diseases" (1).

Gary's first target was the commonly held idea that obesity is simply caused by eating too much and exercising too little, and thus the cure is to eat less and exercise more. He used numerous examples from both humans and animals to show that fat mass is biologically regulated, rather than being the passive result of voluntary behaviors such as eating and exercise. He presented evidence of cultures remaining lean despite a huge and continuous surplus of food, as long as they stayed on their traditional diet. He also described how they subsequently became obese and diabetic on industrial foods (the Pima, for example).

He then moved into what he feels is the biological cause of obesity: excessive insulin keeping fat from exiting fat cells. It's true that insulin is a storage hormone, at the cellular level. However, fat mass regulation involves a dynamic interplay between many different interlacing systems that determine both overall energy intake and expenditure, as well as local availability of nutrients at the tissue level (i.e., how much fat gets into your fat tissue vs. your muscle tissue). I think the cause of obesity is likely to be more complex than insulin signaling.

He also offered the "carbohydrate hypothesis", which is the idea that carbohydrate, or at least refined carbohydrate, is behind the obesity epidemic and perhaps other metabolic problems. This is due to its ability to elevate insulin. I agree that refined carbohydrate, particularly white flour and sugar, is probably a central part of the problem. I'm also open to the possibility that some people in industrial nations are genuinely sensitive to carbohydrate regardless of what form it's in, although that remains to be rigorously tested. I don't think carbohydrate is sufficient to cause obesity
per se, due to the many lean and healthy cultures that eat high carbohydrate diets*. Gary acknowledges this, and thinks there's probably another factor that's involved in allowing carbohydrate sensitivity to develop, for example excessive sugar.

I had the opportunity to speak with Gary at length on Thursday, as well as on Friday at dinner. Gary is a very nice guy-- a straightforward New York personality who's not averse to a friendly disagreement. In case any of you are wondering, he looks good. Good body composition, nice skin, hair and teeth (apologies to Gary for the analysis). Philippe and his wife took us out to a very nice restaurant, where we had a leisurely four-hour meal, and Dr. Mike Eades was in town so he joined us as well. Mike has a strong Southern accent and is also a pleasant guy. Philippe and his wife are generous and engaging people. It was a great evening. The restaurant was nice enough that I wasn't going to be picky about the food-- I ate everything that was put in front of me and enjoyed it.

* I'm talking about prevention rather than cure here. I acknowledge that many people have had great success losing fat using low-carbohydrate diets, including two gentlemen I met on Thursday.

Thursday, April 15, 2010

Copper in Food

Sources of Copper

It isn't hard to get enough copper-- unless you live in an industrial nation. I've compiled a chart showing the copper content of various refined and unrefined foods to illustrate the point. The left side shows industrial staple foods, while the right side shows whole foods. I've incorporated a few that would have been typical of Polynesian and Melanesian cultures apparently free of cardiovascular disease. The serving sizes are what one might reasonably eat at a meal: roughly 200 calories for grains, tubers and whole coconut; 1/4 pound for animal products; 1/2 teaspoon for salt; 1 cup for raw kale; 1 oz for sugar.

Note that beef liver is off the chart at 488 percent of the USDA recommended daily allowance. I don't know if you'd want to sit down and eat a quarter pound of beef liver, but you get the picture. Beef liver is nature's multivitamin: hands down the Most Nutritious Food in the World. That's because it acts as a storage depot for a number of important micronutrients, as well as being a biochemical factory that requires a large amount of B vitamins to function. You can see that muscle tissue isn't a great source of copper compared to other organs, and this holds true for other micronutrients as well.

Beef liver is so full of micronutrients, it shouldn't be eaten every day. Think of it in terms of the composition of a cow's body. The edible carcass is mostly muscle, but a significant portion is liver. I think it makes sense to eat some form of liver about once per week.

Modern Agriculture Produces Micronutrient-poor Foods

The numbers in the graph above come from NutritionData, my main source of food nutrient composition. The problem with relying on this kind of information is it ignores the variability in micronutrient content due to plant strain, soil quality, et cetera.

The unfortunate fact is that micronutrient levels have declined substantially over the course of the 20th century, even in whole foods. Dr. Donald R. Davis has documented the substantial decline in copper and other micronutrients in American foods over the second half of the last century (1). An even more marked decrease has occurred in the UK (2), with similar trends worldwide. On average, the copper content of vegetables in the UK has declined 76 percent since 1940. Most of the decrease has taken place since 1978. Fruits are down 20 percent and meats are down 24 percent.

I find this extremely disturbing, as it will affect even people eating whole food diets. This is yet another reason to buy from artisanal producers, who are likely to use more traditional plant varieties and grow in richer soil. Grass-fed beef should be just as nutritious as it has always been. Some people may also wish to grow, hunt or fish their own food.

Tuesday, April 13, 2010

Interview with John Barban

I recently did a podcast interview with John Barban from the Adonis Lifestyle blog. We talked mostly about fat mass and the body fat "setpoint". As it turns out, what I said must have been at odds with John's philosophy, because he posted another podcast the next week that appears to be about why he disagrees with me!

Anyway, enjoy the interview.

I did another one recently with Jimmy Moore that's coming soon.

Monday, April 12, 2010

Gary Taubes Speaks this Thursday at UW

Gary Taubes will be giving a lecture this Thursday, April 15th, at the University of Washington in Seattle, titled "Why we get fat: adiposity 101 and an alternative hypothesis of obesity". It's free and open to the public. The talk is from noon to 1:00, followed by a question and answer session from 1:00 to 2:00.

The talk will take place in Hogness auditorium, which is room A420 of the Health Sciences building (1959 NE Pacific St). The whole area is difficult to navigate, so allow yourself time to park and find the auditorium. Here are directions to Hogness, including parking.

I'll be sitting near the front if anyone wants to say hi afterward.

Friday, April 9, 2010

Full-fat Dairy for Cardiovascular Health

I just saw a paper in the AJCN titled "Dairy consumption and patterns of mortality of
Australian adults
". It's a prospective study with a 15-year follow-up period. Here's a quote from the abstract:
There was no consistent and significant association between total dairy intake and total or cause-specific mortality. However, compared with those with the lowest intake of full-fat dairy, participants with the highest intake (median intake 339 g/day) had reduced death due to CVD (HR: 0.31; 95% confidence interval (CI): 0.12–0.79; P for trend = 0.04) after adjustment for calcium intake and other confounders. Intakes of low-fat dairy, specific dairy foods, calcium and vitamin D showed no consistent associations.
People who ate the most full-fat dairy had a 69% lower risk of cardiovascular death than those who ate the least. Otherwise stated, people who mostly avoided dairy or consumed low-fat dairy had more than three times the risk of dying of coronary heart disease or stroke than people who ate the most full-fat diary.

Contrary to popular belief, full-fat dairy, including milk, butter and cheese, has never been convincingly linked to cardiovascular disease. In fact, it has rather consistently been linked to a lower risk, particularly for stroke. What has been linked to cardiovascular disease is milk fat's replacement, margarine. In the Rotterdam study, high vitamin K2 intake was linked to a lower risk of fatal heart attack, aortic calcification and all-cause mortality. Most of the K2 came from full-fat cheese. In my opinion, artisanal cheese and butter made from pasture-fed milk are the ultimate dairy foods.

From a 2005 literature review on milk and cardiovascular disease in the EJCN:
In total, 10 studies were identified. Their results show a high degree of consistency in the reported risk for heart disease and stroke, all but one study suggesting a relative risk of less than one in subjects with the highest intakes of milk.

...the studies, taken together, suggest that milk drinking may be associated with a small but worthwhile reduction in heart disease and stroke risk.

...All the cohort studies in the present review had, however, been set up at times when reduced-fat milks were unavailable, or scarce.
The fat is where the vitamins A, K2, E and D are. The fat is where the medium-chain triglycerides, butyric acid and omega-3 fatty acids are. The fat is where the conjugated linoleic acid is. So the next time someone admonishes you to reduce your dairy fat intake, what are you going to tell them??

Tuesday, April 6, 2010

Copper and Cardiovascular Disease

In 1942, Dr. H. W. Bennetts dissected 21 cattle known to have died of "falling disease". This was the name given to the sudden, inexplicable death that struck herds of cattle in certain regions of Australia. Dr. Bennett believed the disease was linked to copper deficiency. He found that 19 of the 21 cattle had abnormal hearts, showing atrophy and abnormal connective tissue infiltration (fibrosis) of the heart muscle (1).

In 1963, Dr. W. F. Coulson and colleagues found that 22 of 33 experimental copper-deficient pigs died of cardiovascular disease. 11 of 33 died of coronary heart disease, the quintessential modern human cardiovascular disease. Pigs on a severely copper-deficient diet showed weakened and ruptured arteries (aneurysms), while moderately deficient pigs "survived with scarred vessels but demonstrated a tendency toward premature atherosclerosis" including foam cell accumulation (2). Also in 1963, Dr. C. R. Ball and colleagues published a paper describing blood clots in the heart and coronary arteries, heart muscle degeneration, ventricular calcification and early death in mice fed a lard-rich diet (3).

This is where Dr. Leslie M. Klevay enters the story. Dr. Klevay suspected that Ball's mice had suffered from copper deficiency, and decided to test the hypothesis. He replicated Ball's experiment to the letter, using the same strain of mice and the same diet. Like Ball, he observed abnormal clotting in the heart, degeneration and enlargement of the heart muscle, and early death. He also showed by electrocardiogram that the hearts of the copper-deficient mice were often contracting abnormally (arrhythmia).

But then the coup de grace: he prevented these symptoms by supplementing the drinking water of a second group of mice with copper (4). In the words of Dr. Klevay: "copper was an antidote to fat intoxication" (5). I believe this was his tongue-in-cheek way of saying that the symptoms had been misdiagnosed by Ball as due to dietary fat, when in fact they were due to a lack of copper.

Since this time, a number of papers have been published on the relationship between copper intake and cardiovascular disease in animals, including several showing that copper supplementation prevents atherosclerosis in one of the most commonly used animal models of cardiovascular disease (6, 7, 8). Copper supplementation also corrects abnormal heart enlargement-- called hypertrophic cardiomyopathy-- and heart failure due to high blood pressure in mice (9).

For more than three decades, Dr. Klevay has been a champion of the copper deficiency theory of cardiovascular disease. According to him, copper deficiency is the only single intervention that has caused the full spectrum of human cardiovascular disease in animals, including:
  • Heart attacks (myocardial infarction)
  • Blood clots in the coronary arteries and heart
  • Fibrous atherosclerosis including smooth muscle proliferation
  • Unstable blood vessel plaque
  • Foam cell accumulation and fatty streaks
  • Calcification of heart tissues
  • Aneurysms (ruptured vessels)
  • Abnormal electrocardiograms
  • High cholesterol
  • High blood pressure
If this theory is so important, why have most people never heard of it? I believe there are at least three reasons. The first is that the emergence of the copper deficiency theory coincided with the rise of the diet-heart hypothesis, whereby saturated fat causes heart attacks by raising blood cholesterol. Bolstered by some encouraging findings and zealous personalities, this theory took the Western medical world by storm, for decades dominating all other theories in the medical literature and public health efforts. My opinions on the diet-heart hypothesis aside, the two theories are not mutually exclusive.

The second reason you may not have heard of the theory is due to a lab assay called copper-mediated LDL oxidation. Researchers take LDL particles (from blood, the same ones the doctor measures as part of a cholesterol test) and expose them to a high concentration of copper in a test tube. Free copper ions are oxidants, and the researchers then measure the amount of time it takes the LDL to oxidize. I find this assay tiresome, because studies have shown that the amount of time it takes copper to oxidize LDL in a test tube doesn't predict how much oxidized LDL you'll actually find in the bloodstream of the person you took the LDL from (10, 11).

In other words, it's an assay that has little bearing on real life. But researchers like it because for some odd reason, feeding a person saturated fat causes their LDL to be oxidized more rapidly by copper in a test tube, even though that's not the case in the actual bloodstream (12). Guess which result got emphasized?

The fact that copper is such an efficient oxidant has led some researchers to propose that copper oxidizes LDL in human blood, and therefore dietary copper may contribute to heart disease (oxidized LDL is a central player in heart disease-- read more here). The problem with this theory is that there are virtually zero free copper ions in human serum. Then there's the fact that supplementing humans with copper actually reduces the susceptibility of red blood cells to oxidation (by copper in a test tube, unfortunately), which is difficult to reconcile with the idea that dietary copper increases oxidative stress in the blood (13).

The third reason you may never have heard of the theory is more problematic. Several studies have found that a higher level copper in the blood correlates with a higher risk of heart attack (14, 15). At this point, I could hang up my hat, and declare the animal experiments irrelevant to humans. But let's dig deeper.

Nutrient status is sometimes a slippery thing to measure. As it turns out, serum copper isn't a good marker of copper status. In a 4-month trial of copper depletion in humans, blood copper stayed stable, while the activity of copper-dependent enzymes in the blood declined (16). These include the important copper-dependent antioxidant, superoxide dismutase. As a side note, lysyl oxidase is another copper-dependent enzyme that cross-links the important structural proteins collagen and elastin in the artery wall, potentially explaining some of the vascular consequences of copper deficiency. Clotting factor VIII increased dramatically during copper depletion, perhaps predicting an increased tendency to clot. Even more troubling, three of the 12 women developed heart problems during the trial, which the authors felt was unusual:
We observed a significant increase over control values in the number of ventricular premature discharges (VPDs) in three women after 21, 63, and 91 d of consuming the low-copper diet; one was subsequently diagnosed as having a second-degree heart block.
In another human copper restriction trial, 11 weeks of modest copper restriction coincided with heart trouble in 4 out of 23 subjects, including one heart attack (17):
In the history of conducting numerous human studies at the Beltsville Human Nutrition Research Center involving participation by 337 subjects, there had previously been no instances of any health problem related to heart function. During the 11 wk of the present study in which the copper density of the diets fed the subjects was reduced from the pretest level of 0.57 mg/ 1000 kcal to 0.36 mg/1000 kcal, 4 out of 23 subjects were diagnosed as having heart-related abnormalities.
The other reason to be skeptical of the association between blood copper and heart attack risk is that inflammation increases copper in the blood (18, 19). Blood copper level correlates strongly with the marker of inflammation C-reactive protein (CRP) in humans, yet substantially increasing copper intake doesn't increase CRP (20, 21). This suggests that elevated blood copper is likely a symptom of inflammation, rather than its cause, and presents an explanation for the association between blood copper level and heart attack risk.

Only a few studies have looked at the relationship between more accurate markers of copper status and cardiovascular disease in humans. Leukocyte copper status, a marker of tissue status, is lower in people with cardiovascular disease (22, 23). People who die of heart attacks generally have less copper in their hearts than people who die of other causes, although this could be an effect rather than a cause of the heart attack (24). Overall, I find the human data lacking. I'd like to see more studies examining liver copper status in relation to cardiovascular disease, as the liver is the main storage organ for copper.

According to a 2001 study, the majority of Americans may have copper intakes below the USDA recommended daily allowance (25), many substantially so. This problem is exacerbated by the fact that copper levels in food have declined in industrial nations over the course of the 20th century, something I'll discuss in the next post.

Sunday, April 4, 2010

Magnesium and Vitamin D Metabolism

Ted Hutchinson posted a link in the comments section of my last post, pointing to a page on the Vitamin D Council's website where Dr. John Cannell discusses cofactors required for proper vitamin D metabolism. It's actually the site's home page, highlighting how important he feels this matter is. In this case, 'cofactor' simply means another nutrient that's required for the efficient production and use of vitamin D. They include:
  • Magnesium
  • Zinc
  • Vitamin K2
  • Vitamin A
  • Boron
And probably others we aren't yet aware of. On another page, Dr. Cannell links to two papers that review the critical interaction between magnesium status and vitamin D metabolism (1, 2). Here's a quote from the abstract of the second paper:
Magnesium... is essential for the normal function of the parathyroid glands, metabolism of vitamin D and adequate sensitivity of target tissues to [parathyroid hormone] and active vitamin D metabolites. Magnesium deficit is usually associated with hypoparathyroidism, low production of active vitamin D metabolites, in particular 1,25(OH)2 vitamin D3 and resistance to PTH and vitamin D. On the contrary, magnesium excess, similar to calcium, inhibits PTH secretion. Bone metabolism is impaired under positive as well as under negative magnesium balance.
Magnesium status is critical for normal vitamin D metabolism, insulin sensitivity, and overall health. Supplemental magnesium blocks atherosclerosis in multiple animal models (3, 4). Most Americans don't get enough magnesium (5).

The bottom line is that no nutrient acts in a vacuum. The effect of every part of one's diet and lifestyle is dependent on every other part. I often talk about single nutrients on this blog, but my core philosophy is that a proper diet focuses on Real Food, not nutrients. Tinkering with nutritional status using supplements is potentially problematic. Despite what some people might tell you, our understanding of nutrition and human health is currently rather crude-- so it's best to respect the accumulated wisdom of cultures that don't get the diseases we're trying to avoid.

Friday, April 2, 2010

Low Vitamin D: Cause or Result of Disease?

Don Matesz at Primal Wisdom put up a post a few days ago that I think is worth reading. It follows an e-mail discussion between us concerning a paper on magnesium restriction in rats (executive summary: moderate Mg restriction reduces the hormone form of vitamin D by half and promotes osteoporosis). In his post, Don cites several papers showing that vitamin D metabolism is influenced by more than just vitamin D intake from the diet and synthesis in the skin.

Celiac disease patients have low 25(OH)D3, the circulating storage form of vitamin D, which spontaneously corrects on a gluten-free diet. There are numerous suggestions in the medical literature that overweight and sickness cause low vitamin D, potentially confounding the interpretation of studies that find lower levels of illness among people with low vitamin D levels.

Don't get me wrong, I still think vitamin D is important in preventing disease. But it does lead me to question the idea that we should force down huge doses of supplemental vitamin D to get our 25(OH)D3 up to 60, 70 or even 80 ng/mL. When the dosage of supplemental D goes beyond what a tan Caucasian could conceivably make on a day at the beach (4,000 IU?), that's when I start becoming skeptical. Check out Don's post for more.